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Program Pannonia Congress of Pathology Spring Congress of the Austrian, Croatian, Hungarian and Slovenian Societies of Pathology and IAP Divisions Graz, Austria, March 3–6, 2010

Program - K&M Congress · fortgeschrittenen NSCLC mit EGFR M+ Zugelassen als erste orale 1st line Monotherapie des NSCLC mit aktivierenden Mutationen der EGFR-TK1 (EGFR M+) Signifi

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Page 1: Program - K&M Congress · fortgeschrittenen NSCLC mit EGFR M+ Zugelassen als erste orale 1st line Monotherapie des NSCLC mit aktivierenden Mutationen der EGFR-TK1 (EGFR M+) Signifi

Program

Pannonia Congress of Pathology

Spring Congress of the Austrian, Croatian, Hungarian and SlovenianSocieties of Pathology and IAP Divisions

Graz, Austria, March 3–6, 2010

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®

®

Die personalisierte 1st line Therapie beimfortgeschrittenen NSCLC mit EGFR M+

Zugelassen als erste orale 1st line Monotherapie des NSCLC mit aktivierenden Mutationen der EGFR-TK1 (EGFR M+)

Signifi kante Verlängerung des progressionsfreien Überlebens um 3,2 Monate bei fortgeschrittenem NSCLC im Vergleich zur Chemotherapie 1,2

Referenzen: 1. Mok TS, Wu Y-L, Thongprasert S, et al. Gefi tinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Eng J Med 2009; 3612. Carboplatin/Paclitaxel

ID17

75;0

1/20

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Fachkurzinformation siehe Seite 17

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Dear Colleagues!

On behalf of the Presidents of the Austrian, Croatian, Hungarian, andSlovenian Societies of Pathology and the respective Divisions of the IAP wewould like to invite you to attend the Pannonia Congress in Graz Austria,March 4–6, 2010.

The program of the congress is focused on Lung, Head & Neck, and Bone &Soft Tissue tumors. Additional sessions will cover preneoplasia, commoninflammatory processes, and others.

Slide courses have been prepared for these organ topics. A precongressinternet access is provided via the Austrian Society homepage (see below).

We have organized lunch satellite symposia on targeted therapy and theimpact of pathology in this field.

Molecular pathology as a relevant method is included in the presentations.

March 3, two pre-congress laboratory courses have been organized for EGF receptor mutation test methodology and on FISH/CISH/SISH resultinterpretation. The lab courses aim on technicians (EGFR mutation test) andyoung academic colleagues (amplification, translocation in tumor diagnosis).

A social dinner is included in the registration fee and will be held in the OldUniversity of Graz. Since space is limited, seats are given to those, registeredearly on.

The city of Graz is located in the southeastern part of Austria and can easilybe reached by plane – several daily flight connections with Frankfurt, Munich,and Vienna airports and by car, because the highways A2 (Vienna to Villach)and A9 (Slovenian border to Wels) cross in Graz.

The Presidents and Secretaries of the four Societies would be delighted towelcome you here in Graz.

Helmut H. Popper József Timár / Zsuzsa SchaffUlrike Gruber-Moesenbacher Attila Zalatnai

Austrian Society Pathology/IAP Hungarian Society Pathology/IAP

Damir Babic Izidor KernSven Seiwerth Metka Volavsek

Croatian Society Pathology Slovenian Society Pathology & Forensic Medicine

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General Information

Organizing Committee:

Prof. Dr. Helmut Popper and OA Dr. Ulrike Gruber-MösenbacherProf. Dr. József Timár, Prof. Dr. Janina Kulka and Dr. Attila ZalatnaiDr. Izidor Kern and Doc. Dr. Metka VolavsekProf. Dr. Damir Babic and Prof. Dr. Sven Seiwerth

Scientific Faculty

Damir Babic, Croatia Gábor Méhes, HungaryAlfred Beham, Austria Bruno Murer, ItalyElisabeth Bruder, Switzerland Florence Pedeutour, FranceMarco Chilosi, Italy Mario Poljak, SloveniaAnne-Marie Cleton-Jansen, Netherlands Helmut Popper, AustriaPaolo DeiTos, Italy Angelika Reiner-Concin, AustriaJános Fillinger, Hungary Zoltán Sápi, HungaryNina Gale, Slovenia Sven Seiwerth, CroatiaUlrike Gruber-Mösenbacher, Austria Irene Sulzbacher, AustriaCornelia Hauser-Kronberger, Austria Eszter Székely, HungaryIzidor Kern, Slovenia József Timár, HungaryKeith Kerr, United Kingdom József Tóvári, HungaryJanina Kulka, Hungary Laszlo Vass, HungaryBozo Kruslin, Croatia Michael Vesely, AustriaJanez Lamovec, Slovenia Metka Volavsek, SloveniaBernadette Liegl-Atzwanger, Austria Attila Zalatnai, HungarySpomenka Manojlovic, Croatia Nina Zidar, SloveniaMatej Bracko, Slovenia

Course Faculty for Technicians

Iris HalbwedlAndrea HofmannTina ReisenhoferGerlinde Winter

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General Information

Registration and Hotel information

Congress Bureau: On-site Organization:

Karin Lichtenegger Katalin MatrayInstitute of Pathology K&M Congress Ltd.Medical University of Graz H-1028 Budapest, Hidegkuti ut 153.Auenbruggerplatz 25 Phone: +36-1-301-2000A-8036 Graz, Austria Fax: +36-1-301-2001Phone: (+43/316) 380 4418 E-mail: [email protected]: (+43/316) 385 3432E-mail: [email protected]

For Hotel reservation go to www.pathology.at; enter at: PathologInnen andfurther on ÖGP/IAP Tagungen; there you will find Frühjahrstagung 2010.Below you will find the hotel registration online.In addition there are rooms available under specific conditions at theRomantik Park Hotel.

This exclusive hotel is situated in the historical city center of Graz, thewalking distance to the congress site is about 5 to 8 minutes. The hotel’sexcellent restaurant offers sophisticated regional cuisine in an elegantsetting. It also provides a SPA which includes sauna, indoor-pool and fitnessarea. The stylish rooms feature all necessities for a comfortable stay. Theyinclude elegant bathrooms, air condition, cable TV, mini-bar, radio, hair dryerand telephones with data port etc. http://www.parkhotel-graz.at/.

For you as a participant at the Pannonia Congress the Parkhotel will offeryou the following exceptional rates (valid until the end of January):

Comfort Single Room € 101,— a dayDouble Room (double occupation) € 160,— a dayDouble Room (single used) € 117,— a day

The rates include a rich breakfast buffet, free parking on hotel premises, useof the business center and the spa facilities as well as all taxes. Bathrobes areprovided in the room.

If you like to take this opportunity please contact the ROMANTIKPARKHOTEL by telephone, fax or mail:

CODE WORD: PANNONIA 2010Phone: (+43/316) 3630–27Fax: (+43/316) 3630–50E-mail: [email protected]

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General Information

Poster Sessions:

Abstracts for Poster Presentations should be sent to: [email protected] of abstracts will be notified directly via E-mail. Abstracts will bepublished in a supplimentary issue of Pathology & Oncology Research.At the end of the meeting a poster price will be presented to the two bestposters exhibited during the meeting. Poster price jury: J. Timar, S. Seiwerth,S. Lax, N. Gale, M. Volavsek, A. Reiner-Concin, J. Kulka, D. Babic.For the participants DFP certificates or equivalents will be prepared bythe congress bureau.Electronic badges with bar codes are prepared which contain all necessaryinformations about payment and registration to the dinner and lunchseminars. Please present these badges at the entrance to the registrationpeople.Speaker’s preview room is located in the second floor; follow the signs fromthe registration desk.

Exhibition Management:

MAW – Medizinische Ausstellungs- und WerbegesellschaftFreyung 6, 1010 Vienna, AustriaPhone: (+43/1) 536 63-38Fax: (+43/1) 535 60 16E-mail: [email protected]

Dates of the meeting

Precongress Lab Course: March 3, 2010**Institute of Pathology, Microscopy room (FISH,CISH, SISH) and Laboratory for MolecularPathology (mutation analysis)University Hospital, Auenbruggerplatz 25, Graz

Pannonia Congress: March 4–6, 2010Alte UniversitätHofgasse 14 (Freiheitsplatz), Graz

Deadlines:

Early registration fee: January 31, 2010Abstract submission: February 4, 2010Satellite Symposia: January 31, 2010 *Precongress course: January 31, 2010 **** For the Satellite Symposia there will be no extra charge, but a preregistration until

February 1, 2010 is mandatory, because a lunch will be served to those registered. SatelliteSymposia cannot be registered onsite!

** For the precongress courses are limited to 15 persons per half-day, so registration is requiredearly on. Multiple registrations from one Institute will not be possible!

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Registration Before After On siteJanuary 31, 2010 January 31, 2010

Members of national societies € 120.– € 140.– € 150.–

Non-members of national societies € 140.– € 160.– € 170.–

Technicians and accompanying persons € 80.– € 100.– € 100.–

One day ticket excluding dinner € 50.– € 50.– € 50.–

One day ticket excluding dinner for technicians and accompanying persons € 35.– € 35.– € 35.–

Satellite Symposia:Registration mandatory before February 1, 2010 Free of charge Free of charge Free of charge

Precongress course:Registration until January 31, 2010 for one person per institution;Space limited to 15 persons per session Free of charge Free of charge Free of charge

Photographer: Karin Bergmann

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Location Map

Google map of the Inner City of Graz. White arrows mark the Congress venueOld University and the Romantik Park Hotel.

Main Sponsors of the Congress

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Wednesday, March 3, 2010

Laboratory day

Limited number, 15 for each session

BMA (technicians)Organized by Gerllinde WinterIris Halbwedl, Andrea Hofmann, Tina Reisenhofer and Gerllinde Winter

8:30 – 12:00 EGFR mutation testing (Group 1)

13:00 – 16:30 EGFR mutation testing (Group 2)

MD (residents)Organized byCornelia Hauser-Kronberger and Michael Vesely

8:30 – 12:00 FISH/SISH (Group 1)

13:00 – 16:30 FISH/SISH (Group 2)

19:00 Get together party of the participants in the Institute of Pathology, Foyer

18:00 – 19:00 Sitzung der Institutsleiter und des Vorstandesder ÖGP-IAP; Institut für Pathologie,Auenbruggerplatz 25, Graz, BibliothekThema: Wie soll sich das Fach die Pathologie in derÖffentlichkeit darstellen – Wie können wir dies erreichen?Moderator: Dr. Ernest Pichlbauer, Vienna

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Thursday, March 4, 2010

Technics Symposiumchaired byCornelia Hauser-Kronberger and Michael VeselyPresentations 12’ followed by 3’ of discussion

8:15 – 8:30 K-RAS mutation testing of colorectal and lungcarcinomas – an affordable algorythmZita Hegedüs, 2nd Dept. Pathology, Semmelweis University,Budapest

8:30 – 8:45 Molecular profiling of non-small cell lung cancerMojca Strazisar and Damjan Glavac, Institute of Pathology,Medical Faculty Ljubljana

8:45 – 9:00 Protein extraction and protein array from formalin fixedparaffin embedded tissuesHannelore Kothmaier, Institute of Pathology, Medical University Graz

9:00 – 9:15 miRNA detection in fixed tissuesLisa Arzt, Institute of Pathology, Medical University Graz

9:15 – 9:30 Optimal handling of surgical specimen to be suitable formolecular examinationsVioletta Piurkó, 2nd Dept. Pathology, Semmelweis University,Budapest

9:30 – 9:45 In situ hybridization methods to detect Her2Neuamplification of breast carcinomaKatalin Varga, Pathology Dept. National Oncology Institute,Budapest

9:45 – 10:15 COFFEE BREAK

10:15 – 10:30 Tissue microarray applications in pathologyTibor Krenács, Budapest

10:30 – 10:45 Pitfalls in CISH and SISHCornelia Hauser-Kronberger, Institute of Pathology,Hospital and Private University Salzburg

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urs

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Thursday, March 4, 2010

10:45 – 11:00 Pitfalls in FISHMichael Vesely, Institute of Pathology, Hospital Hietzing,Vienna

11:00 – 11:15 EGFR status in non small cell lung cancerMitja Rot, University Clinic of Respiratory and AllergicDiseases Golnik

11:15 – 11:30 Mutation analysis of EGFR and KRAS in daily practiceWolfgang Hulla, Institute of Pathology, Kaiser Franz Josef Hospital, Vienna

11:30 – 11:45 Genetic analysis in MicrobiologyHarald Kirschner, Institute of Pathology, Kaiser Franz Josef Hospital, Vienna

11:45 – 12:00 SHORT BREAK

8:30 – 11:45 Basics in Pathology Entrance level, Press Room

Breast Pathology updateAngelika Reiner-Concin

8:30 – 10:00 Meeting of Pulmonary Office OG2Pathology Working Groupchaired byUlrike Gruber-Mösenbacher

10:00 – 11:30 Meeting of Mikrobiology Office OG2Working Groupchaired byMilo Halabi

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urs

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Thursday, March 4, 2010

Lunch Seminar sponsored by Astra Zenecachaired byHelmut Popper and Damir Babic

EGFR mutation and treatment

12:00 – 12:25 Recommendations for EGFR testing in NSCLCRobert Pirker, Dept. Oncology, Medical University Vienna

12:25 – 12:40 The role of Pathology in diagnosis and treatment of NSCLCKeith Kerr, Institute of Pathology, University of Aberdeen, UK

12:40 – 13:00 Basis for targeted therapy in NSCLC – EGFR and othertargetsMartin Filipits, Cancer Research Institute, Vienna

13:00 – 13:40 Poster Session 1chaired bySigurd Lax and Angelika Reiner-Concin

Symposium on Pulmonary Tumor Pathologychaired byHelmut Popper and József Timár

13:40 – 14:00 The importance of adenocarcinoma subtypingHelmut Popper, Institute of Pathology, Medical University Graz

14:00 – 14:20 Squamous cell carcinoma – variants and markersJános Fillinger and Ibolya Soltész, Korányi NationalPulmonology Institute, Budapest

14:20 – 14:40 Large cell carcinoma variants and the implication fortherapyBruno Murer, Institute of Pathology, Ospedale Dell’ Angelo,Zelarino/Mestre, Italy

14:40 – 15:10 Prognostic and predictive markers in lung carcinomasKeith Kerr, Institute of Pathology, University of Aberdeen, UK

15:10 – 15:40 COFFEE BREAK

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Thursday, March 4, 2010

15:40 – 16:10 Is there a metastatic signature in lung cancer?Marco Chilosi, Dept. Pathology, University of Verona, Italy

16:10 – 16:30 Smears, bronchial biopsies, transthoracic biopsies – are these sufficient for molecular testing?József Tímár, 2nd Dept. of Pathology, Semmelweis University Budapest

16:30 – 16:50 Childhood lung tumorsElisabeth Bruder, Institute of Pathology, University of Basle, Switzerland

16:50 – 17:10 Are there any news from SCLC?Izidor Kern, University Clinic of Respiratory and AllergicDiseases Golnik

17:10 – 18:00 MScope, the use of the educational and clinical modulesPierre Le Fevre, Aurora, Montreal, Canada

Th

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Friday, March 5, 2010

Slide Seminar Interstitial Lung Diseasesorganized and chaired byIzidor Kern and Helmut Popper

8:15 – 8:30 Case 1János Fillinger, National Korányi Institute of Pulmonology,Budapest

8:30 – 8:45 Case 2Elvira Stacher, Institute of Pathology, Medical University Graz

8:45 – 9:00 Case 3Izidor Kern, University Clinic of Respiratory and AllergicDiseases Golnik

9:00 – 9:15 Case 4Gerhard Dekan, Institute of Pathology, Medical University Vienna

9:15 – 9:30 Case 5Georg Hutarew, Institute of Pathology, Hospital and Private University Salzburg

9:30 – 9:45 Case 6Ulrike Gruber-Mösenbacher, Institute of Pathology,Teaching Hospital Feldkirch

9:45 – 10:15 COFFEE BREAK sponsored by the Major of the City of Graz,Mag. Siegfried Nagl

10:15 – 10:30 Case 7Ulrike Setinek, Institute of Pathology, Otto Wagner Hospital, Vienna

10:30 – 10:45 Case 8Ibolya Soltész, National Korányi Institute of Pulmonology,Budapest

10:45 – 11:00 Case 9Sven Seiwerth, Institute of Pathology, University of Zagreb

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Friday, March 5, 2010

11:00 – 11:40 Poster Session 3chaired byJozsef Timár and Metka Volavsek

11:40 – 12:00 SHORT BREAK

Lunch Seminar sponsored by Rochechaired byCord Langner and Felix Offner

12:00 – 12:30 Her2Neu in gastric carcinomasJosef Rüschoff, Pathologie Nordhessen, Kassel, BRD

12:30 – 12:45 Do we need immunohistochemical staining for Her2Neuin breast carcinomas?Josef Rüschoff, Pathologie Nordhessen, Kassel, BRD

12:45 – 13:00 General Discussion

Symposium Head & Neck Pathologychaired byNina Gale and Irene Sulzbacher

13:00 – 13:20 Squamous intraepithelial lesions of the LarynxNina Gale, Institute of Pathology, Medical Faculty Ljubljana

13:20 – 13:40 HPV in upper respiratory tract tumorsMario Poljak, Institute of Microbiology, Medical Faculty Ljubljana

13:40 – 14:00 Spindle cell carcinomas of the Head&NeckNina Zidar, Institute of Pathology, Medical Faculty Ljubljana

14:00 – 14:20 Soft tissue tumors in URTAlfred Beham, Institute of Pathology, Medical University Graz

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Friday, March 5, 2010

14:20 – 14:35 EGFR and functional markers in selecting head and neckcarcinoma patients for Cetuximab and tyrosine kinaseinhibitor treatmentJózsef Tóvári, National Koranyi Institute of TB andPulmonology, National Institute of Oncology, Budapest

14:35 – 14:50 The role of aspiration cytology in the diagnosis of headand neck lumpsEszter Székely and Járay Balázs, 2nd Dept. of Pathology,Semmelweis University, Budapest

14:50 – 15:10 Salivary gland tumorsLaszlo Vass, Dept. Pathology, Flór Ferenc Hospital,Budapest

15:10 – 15:30 Odontogenic cysts and tumorsSpomenka Manojlovic, Institute of Pathology, University of Zagreb

15:30 – 16:00 COFFEE BREAK

Symposium on Soft Tissue & Bone Tumorschaired bySven Seiwerth and Alfred Beham

16:00 – 16:30 Genetics of soft tissue tumorsFlorence Pedeutour, Faculty of Medicine, Laboratory ofSolid Tumor Genetics, Nice University Hospital and CNRSUMR

16:30 – 17:00 The spectrum of myogenic and fibrogenic sarcomasAngelo Paolo DeiTos, Anatomic Pathology, General Hospital of Treviso, Treviso

Fri

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Friday, March 5, 2010

Evening Dinner sponsert by the Governor of Styria,Mag. Franz Voves, Old University Graz

19:30 – 20:00 Welcome Cocktail

Welcome by the Governor of Styria, Mag. Franz Voves

Welcome by the Major of the City of Graz, Mag. Siegfried Nagl

Welcome addresses by the Presidents of the four SocietiesH. PopperJ. TimarD. BabicI. Kern

Between main course and dessert:Diseases in a Stone Age people at the time of firstcontact with 20th century medicineRobin A. Cooke, Editor of IAP News, Australia

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Ask for an eye-opening demonstration of the innovative mScope today. Call toll free: 1-866-343-2646 Fax: 514-664-4767 Email: [email protected]

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Saturday, March 6, 2010

Symposium on Soft Tissue & Bone Tumorscontinued from March 5chaired bySven Seiwerth and Alfred Beham

8:30 – 8:50 Sarcoma – what we need to know about diagnosis andsignaling pathways?Sven Seiwerth, Institute of Pathology, University of Zagreb Synovial

8:50 – 9:10 Targeted therapy in osteosarcoma – fact or fiction?Anne-Marie Cleton-Jansen, Institute of Pathology, Leiden University Medical Center, NL

9:10 – 9:25 Contemporary GIST pathologyBernadette Liegl-Atzwanger, Institute of Pathology,Medical University Graz

9:25 – 9:40 Vascular tumors of soft tissueJanez Lamovec, Institute of Oncology Ljubljana

9:40 – 9:55 Pediatric soft tissue tumorsBozo Kruslin, Institute of Pathology, University of Zagreb

9:55 – 10:10 FISHING OR SISHING in soft tissue tumors?Gábor Méhes, Institute of Pathology, Debrecen

10:10 – 10:30 COFFEE BREAK

Slide Seminar Head & Neck Pathologyorganized and chaired byMetka Volavsek and Lászlo Vass

10:30 – 10:45 Case 1Lászlo Vass, Dept. Pathology, Flór Ferenc Hospital,Budapest

10:45 – 11:00 Case 2Balázs Járay, 2nd Dept. of Pathology, Semmelweis University Budapest

11:00 – 11:15 Case 3Nina Gale, Institute of Pathology, Medical Faculty Ljubljana

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Saturday, March 6, 2010

11.15 – 11:30 Case 4Nina Zidar, Institute of Pathology, Medical Faculty Ljubljana

11:30 – 11:45 Case 5Spomenka Manojlovic, Institute of Pathology, University of Zagreb

11:45 – 12:00 Case 6Metka Volavsek, Institute of Pathology, Medical Faculty Ljubljana

12:00 – 12.15 Case 7Alfred Beham, Institute of Pathology, Medical University Graz

12.15 – 12:30 Case 8Irene Sulzbacher, Medical University of Vienna

Lunch Seminar sponsored by DAKOchaired bySpomenka Manojlovic and Attila Zalatnai

12:30 – 13.10 Diagnostics in the future, a companies perspectiveMark Bloomfield, Country Manager, DAKO

13.10 – 13:30 Quality Management in Her2Neu testingRepresentative from DAKO

Satu

rdayFachkurzinformation zur Umschlagseite 2

BEZEICHNUNG DES ARZNEIMITTELS: IRESSA 250 mg FilmtablettenQUALITATIVE UND QUANTITATIVE ZUSAMMENSETZUNG: Jede Tablette enthält 250 mg Gefitinib. Sonstiger Bestandteil: JedeTablette enthält 163,5 mg Lactose (als Monohydrat). ANWENDUNGSGEBIETE: IRESSA ist angezeigt zur Behandlung von erwach-senen Patienten mit lokal fortgeschrittenem oder metastasiertem, nicht-kleinzelligem Lungenkarzinom (NSCLC) mit aktivierenden Mu-tationen der EGFR-TK (Für weitere Informationen siehe auch Abschnitt 5.1 der veröffentlichten Fachinformation). GEGENANZEIGEN:Überempfindlichkeit gegen den Wirkstoff oder einen der sonstigen Bestandteile. Stillen (Für weitere Informationen siehe auch Ab-schnitt 4.6 der veröffentlichten Fachinformation). PHARMAKOTHERAPEUTISCHE GRUPPE: Proteinkinase-Hemmer; ATC-Code:L01XE02. LISTE DER SONSTIGEN BESTANDTEILE: Tablettenkern: Lactose-Monohydrat, Mikrokristalline Cellulose (E460), Cros-carmellose-Natrium, Povidon (K29-32) (E1201), Natriumdodecylsulfat, Magnesiumstearat (Ph.Eur.). Tablettenhülle: Hypromellose(E464), Macrogol 300, Titandioxid (E171), Eisen(III)-hydroxid-oxid x H2O (E172), Eisen(III)-oxid (E172). INHABER DER ZULASSUNG:AstraZeneca AB, S-151 85, Södertälje, Schweden. VERSCHREIBUNGSPFLICHT/APOTHEKENPFLICHT: NR, apothekenpflichtig.Informationen zu den Abschnitten „Nebenwirkungen“, „Wechselwirkungen mit anderen Arzneimitteln und sonstige We-chselwirkungen“ und „Besondere Warnhinweise und Vorsichtsmaßnahmen für die Anwendung“ sind der veröffentlichtenFachinformation (z.B. Austria Codex) zu entnehmen.

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Saturday, March 6, 2010

Slide Seminar Soft Tissue & Bone Tumorsorganized and chaired byMatej Bracko and Zoltán Sáp

13:30 – 13:45 Case 1Zsolt Orosz, National Institute of Oncology, Budapest

13:45 – 14:00 Case 2Alfred Beham, Medical University Graz

14:00 – 14.15 Case 3Sven Seiwerth, Institute of Pathology, University of Zagreb

14.15 – 14:30 Case 4Susanna Lang, Medical University of Vienna

14:30 – 14:45 Case 5Zoltán Sápi, 1st Dept. of Pathology, Semmelweis University, Budapest

14:45 – 15:00 Case 6Matej Bracko, Department of Pathology, Institute of Oncology, Ljubljana

15:00 – 15.15 Case 7Snjezana Frkovic Grazio, Department of Pathology,Institute of Oncology, Ljubljana

15.15 – 15:30 Case 8Tamás Tornóczky, Dept. Pathology, University of Pécs

15:30 – 15:50 Announcements of the poster awards

15:50 – 16.10 Closing remarks by the Presidents

Satu

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50072 12MAY09

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Besuchen Sie uns an unserem Stand bei derFRÜHJAHRSTAGUNG 2010-PANNONIA

CONGRESS of PATHOLOGYSpring meeting of the Austrian, Croatian, Hungarian

and Slovenian Societies of Pathology and IAP Divisions

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Main Sponsors

AstraZeneca, Wien, ÖsterreichDako, Wien, ÖsterreichRoche Austria, Wien, Österreich

Sponsors

3DHISTECH, Budapest, UngarnBecker Laboreinrichtung, Wien, ÖsterreichExakt Advanced Technologies, Norderstedt, DeutschlandBioProducts Mag. Th. Langmann, Großmugl, ÖsterreichDCS Innovative Diagnostik-Systeme, Hamburg, DeutschlandEubio, Wien, ÖsterreichGRZ IT Center Linz, Linz, ÖsterreichHamamatsu Photonics, Herrsching, DeutschlandHistocom Medizin Technik, Wiener Neudorf, ÖsterreichHVD Life Science, Wien, ÖsterreichLeica Mikrosysteme, Wien, ÖsterreichMedite, Maishofen, ÖsterreichA. Menarini Diagnostics, Wien, ÖsterreichMerck Serono, Wien, ÖsterreichMTM Laboratories, Heidelberg, DeutschlandNikon, Wien, ÖsterreichQiagen, Hilden, DeutschlandRoche Diagnostics, Wien, ÖsterreichSanova Pharma, Wien, ÖsterreichStradis, Sierndorf, ÖsterreichTissueGnostics, Wien, Österreich

Die Tagung wird unterstützt vom

Landeshauptmann der Steiermark,

Mag. Franz Voves, der Abt. 3 Wissenschaft

und Forschung, und vom Bürgermeister

der Stadt Graz, Mag. Siegfried Nagl

20

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Abstract No 1/1

MALT lymphoma arising from Hashimoto’s thyreoiditis: a benign lymphoproliferative disorder?

Names and affiliations Mail address of presenter: Tamás Csonka, Ferenc Fazakas,Balázs Dezs, Gábor Méhes Department of Pathology, University of Debrecen, Nagyerdei krt. 98., H-4032 Debrecen, Hungary

Introduction:The B-cell marginal zone lymphomas of the thyroid gland are rare and develop fromreactive lymphoid hyperplasia associated to Hashimoto's thyroiditis. We report on a80-year-old female patient who had a bilateral subtotal thyroidectomy in July 2000which was diagnosed as Hashimoto’s thyreoiditis after histology. Nine years later shecomplained a goiter of the residual thyroid gland. The CT scan of the neck regionshowed a large right thyroid lobe compressing the trachea.

Methods and results:The removed tissue presented histologically large areas of hyperplastic lymphoid tissue with frequent secondary follicles and an expanded marginal zone. The numberof thyroid follicules was decreased and many of them were filled with small compactmonocytoid cell balls. While the diffuse lymphatic infiltrate was a mixture of B- andT-cell populations and plasmocytes according to the IHC profile, the intrafollicularmonocytoid cells showed homogenous intense postivity for CD20 and CD79a andnegativity for CD5, cyclin D1 and Bcl-2. The Mib-1 cell proliferation marker corrobo-rated the impression of an indolent neoplasm with staining of only 2% of the intrafollicular B cells, while up to 20% cell proliferation was observed in the hyper-plastic lymphoid infiltrate of the thyroid. To prove the monoclonal neoplastic natureof the lymphoprolifertive change we examined the immunoglubulin heavy chain (IgH)fraction (FR) 2 and 3 with polimerase chain reaction (PCR), which showed a polyclonal arrangement when whole tissue sections were applied. However, lasercapture microdissection (LCM) of the intrafollicular B cell balls showed a monoclonalIgH arrangement for both FR2 and FR3. The diagnosis of an indolent marginal zonelymphoma arising from Hashimotho's thyroiditis was stated. Following the review ofthe surgical specimen removed in the year 2000 we were able to find isolated fociof monocytoid B-cells in an infiltrative intrafollicular fashion identical to the change9 years later.

Conclusion:Lymphoid hyperplasia in Hashimoto’s thyreoiditis may cover benign clonal lympho-proliferative changes of MALT origin which persist for extreme long time periodswithout transformation Extranodal MALT lymphoma of the thyroid seems to evolvefrom this cell population without systemic dissemination in a very slow fashion.

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Abstract No 1/2

A case of colon cancer with multiple K-Ras mutations andcorresponding clonal segregation to different lymph nodemetastases

Names and affiliations Mail address of presenter:Jahn SW1, Stacher E1, Stockinger R2, Spreitzer S2, Offner F2, Höfler G1

1 Department for Pathology, Medical University of Graz2 Department for Pathology, LKH Feldkirch

Stephan Jahn: [email protected]

Introduction:K-Ras mutation status analysis in colorectal cancer has gained paramount impor-tance in predicting response to humanized antibody treatment targeting the EGFR-receptor. Few publications have addressed the question of intratumoral heterogeneityand corresponding patterns of metastatic spread. High concordance rates betweenprimary tumour and metastases are the almost universal finding in the literature.

Methods:We investigated a case of colon cancer from a 60year old male with a moderately differentiated tubular adenocarcinoma of the coecum pT4pN2 (4/20 lymph nodes).A predominant mucinous tumour differentiation of the primary tumour was observedwith one adjacent area demonstrating a non-mucinous tubular differentiation. A corresponding non-mucinous tumor differentiation was noted in one lymph nodemetastasis while three lymph node metastases showed signs of a mucinous diffe -rentiation. Material from primary tumour as well lymph node metastases was se-lected by laser capture microdissection. Tumour DNA was analyzed for K-Rasmutations by allele specific PCR (ARMS) using the TheraScreen: K-RAS Mutation Kit™(DxSR) on 31300 Avant Genetic Analyzer™s (Applied BiosystemsR) and/or Pyrose-quencing (PyroMark KRAS Kit™, QiagenR on a PyroMark Q24™ sequencer, QuiagenR).

Results:Intratumoral heterogeneity of K-ras mutation was observed with adjacent areasdemonstrating monoclonal mutations at codon 12 of the K-ras gene consisting ofGGT->GAT and GGT->GTT mutations respectively. One lymph node metastasis demon-strated clonal GGT->GTT mutation as opposed to three lymph node metastases withclonal GGT-GAT mutation. Furthermore GGT->GAT mutated tumour areas were asso-ciated with mucinous differentiation in both primary tumour and metastases as opposed to GGT->GTT mutated tumour areas with a non-mucinous phenotype.

Discussion and Conclusion:Colorectal adenocarcinoma can demonstrate intratumoral heterogeneity with regardto K-Ras mutational status. Heterogeneity not only applies to mutation versus wild-type heterogeneity but also to the specific type of K-Ras mutation present. Multipledifferent K-Ras mutations can clonally segregate to different lymph node metastases,which points to K-Ras mutations taking place prior to metastatic spread. Multiple dif-ferent K-Ras mutations in (lymph)node metastases are not necessarily a sign of mul-tiple primary malignancies. Although therapeutic management is currently notstratified according to the type of K-Ras mutation detected, future therapies mightbe targeted to specific K-Ras mutations. Detection of K-Ras mutation heterogeneitymight, therefore, gain therapeutic importance.

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Abstract No 1/3

Tumour Size – an Underestimated Prognostic Variable in Colorectal Cancer?

Marion J. Pollheimer,1 Peter Kornprat,2 Richard A. Lindtner,1 Andrea Schlemmer,3

Peter Rehak,4 and Cord Langner1

1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 Graz, Austria

2 Department of Surgery, Division of General Surgery, Medical University of Graz,Auenbruggerplatz 29, A-8036 Graz, Austria

3 Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Auenbruggerplatz 2, A-8036 Graz, Austria

4 Department of Surgery, Research Unit for Biomedical Engineering & Computing,Medical University of Graz, Auenbruggerplatz 29, A-8036 Graz, Austria

E-mail address of presenter: [email protected]

Introduction:T classification, reflecting vertical tumour penetration across the different layers ofthe bowel wall, remains the strongest prognostic parameter in colorectal cancer(CRC). Our study aimed to investigate the clinical significance of tumour size, in particular the maximum horizontal tumour diameter, in a large cohort of CRC patients.

Methods:400 patients were randomly sampled from the files of the CRC database of the Institute of Pathology, Medical University of Graz, Austria. Of these, 381 tumours wereavailable for review pathology. Tumour size and location were extracted from themedical history and were known for 359 patients (94%). 107 tumours (28%) were located in the right colon, 110 (29%) in the left colon, and 164 (43%) in the rectum.Receiver-operator characteristic (ROC) analysis was applied to identify the optimal(maximum of sum of sensitivity and specificity) cut-off values with respect to prognostic impact.

Results:Median tumour size was 4.5 cm (range 0.6-15). Tumour size exceeding 4.5 cm was observed in 159 patients (44%) and was associated with high T and N classification,high UICC stage and poor tumour differentiation. At median follow-up of 59 months,141 patients (40%) showed tumour progression. While 4.5 cm was identified as theoptimal prognostic cut-off value within the whole group of patients, ROC analysis restricted to different parts of the large bowel determined 5 cm, 5.3 cm, 3.9 cm, and3.4 cm as cut-off values with the strongest discriminatory capacity in colon, right-sided colon, left-sided colon, and rectum cancers, respectively. Within the colon,tumour size exceeding 5 cm proved to be a significant prognostic variable in both univariate and multivariate analyses with respect to prediction of progression-free(RR 2.09, 95% CI 1.25-3.48, p=0.005) and cancer-specific survival (RR 1.86, 95% CI1.08-3.21, p=0.025). In subgroup analyses applying the above mentioned optimal cut-off values, prognostic impact was particularly strong in right-sided cancers compared with left-sided cancers. Regarding rectal cancers, no independent influence on outcome was noted.

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Abstract No 1/3

Discussion and Conclusion:Tumour size, in particular the maximum horizontal tumour diameter, proved to bean important prognostic parameter for patients with CRC. Optimal cut-off valuesvary among different parts of the large bowel, decreasing from the right colon tothe left, and ultimately to the rectum. While prognostic impact is strong within thecolon, it appears to be of minor value within the rectum. Since tumour size is sig-nificantly associated with progression-free and cancer-specific survival it may beof importance with respect to surveillance and selection of patients for adjuvanttherapy.

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Abstract No 1/4

Colorectal Cancer: “Epithelial-Epithelial-Transition (EET)” atthe Invasive Front

Authors and affiliations:Lars Harbaum, 1 Marion J. Pollheimer, 1 Peter Kornprat, 2 Richard A. Lindtner, 1 Andrea Schlemmer, 3 Peter Rehak, 4 and Cord Langner11 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036

Graz, Austria 2 Department of Internal Medicine, Division of Oncology, Medical University of Graz,

Auenbruggerplatz 15, A-8036 Graz, Austria 3 Department of Surgery, Division of General Surgery, Medical University, Austria

Auenbruggerplatz 29, A-8036 Graz, Austria4 Institute for Medical Informatics, Statistics and Documentation,

Medical University of Graz, Auenbruggerplatz 2, A8036 Graz, Austria5 Department of Surgery, Research Unit for Biomedical Engineering & Computing,

Medical University of Graz, Auenbruggerplatz 29, A-8036 Graz, Austria

E-Mail address of corresponding author: [email protected]

E-Mail address of presenting author: [email protected]

Introduction:Non-neoplastic colorectal mucosa as well as colorectal adenoma and/or carcinomagenerally lack expression of keratin 7 (K7). Recent evidence, however, indicates thatsome colorectal tumours acquire K7 expression during the neoplastic process. Thisstudy aimed to assess the prevalence of K7 expression in colorectal cancer (CRC), tocorrelate findings with clinicopathological parameters and outcome of affected pa-tients, and to evaluate the distribution of K7 expressing cells within tumour tissues.

Methods:400 patients were randomly sampled from the files of the CRC database of the Institute of Pathology, Medical University of Graz, Austria. Of these, 370 patientswere evaluated for K7 expression by immunohistochemistry using a tissue microar-ray technique and in an additional step by whole section staining. Follow-up datawere available for 340 (92%) patients. K7 expression was semiquantitatively scoredas either focal (<10%), moderate (10-50%), or extensive (>50%). K7 expression wasrelated to various clinicopathological parameters as well as progression-free and cancer-specific survival.

Results:32 (9%) tumours were immunoreactive for K7, with 5 cases showing extensive, 4 moderate and 23 focal expression, respectively. K7 expression prevailed in singlecells and small cell clusters at the invasion front and was associated with the amountof tumour budding, 20/158 (13%) tumours with high degree of tumour budding (≥10budding foci at x20 objective lens) showed K7 expression compared with 12/212 (6%)tumours with low degree of tumour budding (p=0.02). In addition, K7 expression wassignificantly associated with poor tumour differentiation, since 18 out of 119 (16%)high grade (G3/G4), yet only 14 out of 251 (6%) low grade (G1/G2) cancers showed K7immunoreactivity (p=0.005).

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Abstract No 1/4

Disease progression occurred in 15/29 (52%) patients with K7-positive tumours and126/311 (41%) patients with K7-negative tumours (p=0.19, log-rank test). Actuarial 5-year progression-free survival rates for patients with K7-positive and patients withK7-negative tumours were 43% and 60%, respectively. Moreover, 14/29 (48%) patients with K7-positive tumours, yet only 103/311 (33%) patients with K7-negativetumours died of disease (p=0.06, log-rank test). Actuarial 5-year cancer-specific survival rates for patients with K7-positive and patients with K7-negative tumourswere 51% and 66%, respectively.

Discussion and Conclusion:K7 expression is rarely observed in colorectal cancer and is, if present, usually foundonly in a minority of tumour cells. Remarkably, however, K7-positive tumour cellswere found to cluster at the invasive front, correlating with the amount of tumourbudding. These changes in the keratin composition of the cytoskeleton illustrate hitherto unrecognized morphological changes occurring during the process of invasion and may, in accordance to the well established concept of epithelial-mesenchymal transition (EMT), tentatively be named “epithelial-epithelial transition(EET)”.

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Abstract No 1/5

Prognostic Significance of Tumour Necrosis in Colorectal Cancer

Marion J. Pollheimer1, Peter Kornprat2, Richard A. Lindtner1, Andrea Schlemmer3, Peter Rehak4, and Cord Langner1

1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 Graz, Austria

2 Department of Surgery, Division of General Surgery, Medical University of Graz,Auenbruggerplatz 29, A-8036 Graz, Austria

3 Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Auenbruggerplatz 2, A-8036 Graz, Austria

4 Department of Surgery, Research Unit for Biomedical Engineering & Computing,Medical University of Graz, Auenbruggerplatz 29, A-8036 Graz, Austria

E-Mail address of presenter: [email protected]

Introduction:The prognostic impact of tumour necrosis in colorectal cancer (CRC) is still underdebate. Our study aimed to evaluate the prognostic significance of tumour necrosiswith respect to progression-free and cancer-specific survival in a large cohort of patients and to relate findings to the expression of proteins involved in the controlof cancer cell death, such as p53 and bcl-2.

Methods:381 cancer specimens were retrospectively re-evaluated. Follow-up data were available from 350 (92%) patients, mean and median time of follow-up being 64 and61 months, respectively. The extent of tumour necrosis was semiquantitatively assessed and recorded as either absent, focal (<10% of the tumour area), moderate(10-30%) or extensive (>30%). Findings were correlated with different clinicopatho-logical parameters as well as the expression of p53 and bcl-2 which was assessed immunohistochemically using a tissue microarray technique and recorded as eitherpositive (using a cut-off value of 10%) or negative.

Results:Tumour necrosis was noted in 365 (96%) tumours, with 180 (47%) cases showingfocal necrosis, 119 (31%) moderate necrosis, and 66 (17%) extensive necrosis, respectively. Extent of necrosis was significantly associated with high T classifica-tion (p<0.001), high N classification (p=0.005), high UICC stage (p<0.001), poor tumour differentiation (p<0.001), large tumour size (p<0.001), and presence of bloodvessel invasion (p=0.01). Regarding TMA analysis, cancer tissue allowing a reliableevaluation of p53 and bcl-2 immunoreactivity was present in 368 (97%) cases. Distinct nuclear p53 immunoreactivity was observed in 192 (52%) tumours, whereasdistinct cytoplasmic bcl-2 immunoreactivity was present in 95 (26%) tumours. We observed no association of tumour necrosis with the expression of p53 and bcl-2.In Kaplan-Meier analyses using cut-off values of 10% and 30% for assessment of tumour necrosis, prognostic impact was observed regarding both progression-freeand cancer-specific survival (p<0.001), respectively. Multivariate testing, however,proved only the 30% cut-of value (extensive necrosis) as independent predictor ofboth disease progression and cancer-specific survival in a model including a collection of well established prognosticators, such as T and N classification and tumour grade. Of note, restricting analysis to UICC stage II patients, only the 10%cut-off value for tumour necrosis proved to be an independent prognostic variablewith respect to progression-free, yet not with respect to cancer-specific survival.

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Abstract No 1/5

Discussion and Conclusion:Tumour necrosis is a common finding in CRC, and its extent is significantly associatedwith T and N classification, UICC stage, tumour size and grade as well as angioinva-sion. In addition, tumour necrosis proved to be an independent prognostic parameterwith respect to both progression-free and cancer-specific survival. Since tumour necro-sis is readily assessable in H&E stained sections, its presence should routinely be com-mented upon in the pathology report.

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Abstract No 1/6

Squamous cell carcinoma of the lung with extensive basementmembrane material deposition: report of a case

Names and affiliations: Ulamec M*, Demirovi A*, Br i L**, Pa i A**, Krušlin B*.

* Ljudevit Jurak Department of Pathology, Sestre milosrdnice University Hospital,Vinogradska 29, 10000 Zagreb

** Department of Pathology, School of Medicine, University of Zagreb, 10000 Zagreb

E-Mail address of presenter: [email protected]

Lung cancer is one of the most common cancers in the world and one with the highest mortality rate. Squamous cell carcinomas comprise 44% of lung cancers inmen, and 25% in women. Disease stage and performance status at diagnosis are themost powerful prognostic signs but histologic subtype and growth patterns are alsoimportant. Basement membrane is important in regulation of cell growth and diffe -ren tiation. The loss of an intact basal membrane is the initial step in tumor invasion.Carcinomas of different origin with abundant basement membrane depositions weredescribed in the literature. It seems that the patients with extensive basal membranedepositions have favorable prognosis and it might have value as an additional independent prognostic indicator for survival. We describe male patient, 71 years old,with squamous cell carcinoma of the lung, in stage I of the disease. Tumor measured5 cm in greatest dimension and was in proximity of main bronchus, without lymphnode metastases. Microscopically, tumor was composed of cords and nests of poorlydifferentiated atypical squamous cells, focally with central necrosis. Around tumorsnests and in the adjacent tissue massive basal membrane deposits were found. Deposits were more clearly seen with AlcianPAS and Mallory staining. According to the literature data, well differentiated tumors showed extensive basement membrane deposition and in our case abundant deposits surroundedpoorly differentiated atypical squamous cells.

Literature: Velde GPM et al. Prognostic significance of basement membrane deposition in operable squamous cell carcinomas of the lung. Cancer. 1991;67:3001-5.Hagedorn HG et al. Synthesis and degradation of basement membranes and extra-cellular matrix and their regulation by TGF-beta in invasive carcinomas. Int J Oncol.2001; 18:669-81Havenith MG et al. Type IV collagen immunoreactivity in colorectal cancer. Prognostic value of basement membrane deposition. Cancer 1988;62:2207-11.Conn IG et al. Basement membranes in urothelial carcinoma. Br J Urol 1987;60:536-42

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Abstract No 1/7

Gastric Cancer and Concomitant Renal Cell Carcinoma – A Systematic Immunohistochemical and Molecular Analysis

Johannes Betge,1 Marion J. Pollheimer,1 Andrea Schlemmer,2 Gerald Hoefler,1 andCord Langner1

1 Institute of Pathology, Medical University of Graz, Graz, Austria2 Institute for Medical Informatics, Statistics and Documentation,

Medical University of Graz, Graz, Austria

E-Mail address of corresponding author: [email protected]

E-Mail address of presenting author: [email protected]

Introduction:Our study aimed to evaluate 12 patients with concomitant gastric cancer and renalcell carcinoma (RCC) including conventional histology, immunohistochemistry as wellas molecular analysis.

Methods:Clinicopathological and follow-up data were analyzed by chart review and interviewing attending physicians. Basic personal data were compared with that ofpatients experiencing either gastric cancer or RCC contained in the files of our institute. Histopathology of all tumor probes was reassessed. Immunohisto-chemistry included p53 expression, proliferative activity (MIB-1), mismatch repair status and E-Cadherin expression for gastric cancers which were additionally analyzed for Epstein-Barr-Encoded-RNA (EBER) by in-situ hybridization (ISH). MSIwas analyzed with a PCR multiplex system and capillary electrophoresis. KRAS mutations in codons 12 and 13 were tested by pyrosequencing.

Results:There were eight males and four females. Time of diagnosis was not significantlyearly for both cancers. Two patients had additional primary colorectal carcinomas(CRCs). The majority of gastric cancers were poorly differentiated with tumor infiltrating lymphocytes (TILs) being a common finding. All RCCs were of clear celltype, mostly well differentiated and were diagnosed in an early stage. Gastric cancerswere rapidly proliferating (MIB-1) ands showed loss of E-cadherin staining in a significant number of cases. Two gastric cancers had a loss of mismatch repair proteins hMLH1 and PMS2, which was confirmed by molecular analysis showing ahigh degree of microsatellite instability. All RCCs were microsatellite stable. EBV wasdetected by ISH in one gastric cancer. Pyrosequencing for detection of KRAS mutations was positive in one gastric cancer. Two patients had also KRAS mutationsin additional CRCs, while none of the RCCs had KRAS mutations.

Discussion and Conclusion:Gastric carcinomas had striking histological features in terms of poor differentiationand presence of TILs. In contrast to other studies, this particular phenotype is not related to molecular events indicating defective DNA repair or EBV infection in thesepatients. A coherent cause in molecular carcinogenesis with the concomitant RCCswas not proven in this study.

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Abstract No 1/8

Intrathyroid thyroglossal duct cyst – case report

Names and affiliations: Demirovi A1, Pažanin L1, Džepina D2, Ulamec M1, Krušlin B1

1 University Department of Pathology, Sestre milosrdnice University Hospital, Zagreb, Croatia

2 Department of Otorynolaringology, Sestre milosrdnice University Hospital, Zagreb, Croatia

E-Mail address of presenter: [email protected]

Introduction: Thyroglossal duct cysts are cystic dilatations of epithelial remnants of the thyro-glossal duct tract formed during the migration of the thyroid during embryogenesis.Most patients present as children, although presentation at any age is possible. Thesecongenital lesions present most commonly as midline neck masses at the level ofthe thyrohyoid membrane and are closely associated with the hyoid bone, but theyhave been also reported in atypical locations. There have been few reported cases ofintrathyroid thyroglossal duct cyst. We report a case of an intrathyroid thyroglossalduct cyst presenting as a painful mass in the lateral neck.

Case report: A 37-year-old male presented with a painful, left lateral neck mass that was clinicallyindistinguishable from a thyroid nodule. Ultrasound revealed a cystic lesion of theleft thyroid lobe. Findings of ultrasound-guided fine-needle aspiration biopsy wereconsistent with inflammatory changed cystic lesion. After the antibiotic therapy, themass was less painful but reduced in size insignificantly. The patient was admitted forthe surgical treatment and left thyroid lobectomy was performed. Gross examina-tion of the thyroid lobe revealed a well defined cystic lesion, 2.5 cm in diameter, filled with white to yellow granular content. Microscopically, the cyst wall was partially lined with flattened, nonkeratinizing squamous epithelium. The lining epithelium was, however, mostly desquamated and replaced by the granulation tis-sue rich in mononuclear inflammatory cells, hystiocytes, macrophages and sidero-phages. The cyst was completely embedded within the thyroid gland and no tractwas found.The surrounding parenchyma consisted of variably sized thyroid follicleslined with normal-looking thyreocytes. The pathological findings were consistent withintrathyroid thyroglossal duct cyst, in this case secondarily changed due to inflam-mation.

Discussion: Thyroglossal duct cysts are congenital lesions that usually develop in the midline ofthe neck. They can be unlined or lined with pseudostratified, ciliated columnar respiratory epithelium or a nonkeratinizing squamous epithelium. Atypical presen-tations include tongue, suprasternal and thyroid locations. In the review of the literature we found eight reported cases of thyroglossal duct cyst located in the thyroid. These cysts are usually asymptomatic but symptoms can include cough, intermittent choking, shortness of breath or pain due to infection. In this case the patient presented with a painful mass in the lateral neck and findings of ultrasound-guided fine-needle aspiration biopsy were consistent with inflammatory changed cystic lesion. The cytology of the aspirated material was useful in distinguishing the

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Abstract No 1/8

lesion from other entities such as carcinoma with cystic changes, dermoid cyst, thymic cyst and other cystic lesions. However, final diagnosis was set after the patohistological evaluation of the surgically removed thyroid lobe. This case descri-bes the atypical location of the thyroglossal duct cyst and suggests that intrathyroidthyroglossal duct cyst should be included in the differential diagnosis of patients withcystic thyroid lesions.

Literature: R. Johnston, J.L. Wei, J. Maddalozzo, Intra-thyroid thyroglossal duct cyst as a diffe-rential diagnosis of thyroid nodule. Int J Pediatr Otorhinolaringol, 2003;67:1027-30A. Shifrin, J. Vernick, A thyroglossal duct cyst presenting as a thyroid nodule in thelateral neck. Thyroid, 2008;2:263-5

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Abstract No 1/9

The Cytokine Receptor Superfamily Serves as a PromisingTherapeutic Target in Colorectal Cancer – Which Prospects Arise from the Prolactin Receptor?

Authors and affiliations:Lars Harbaum1, Marion J. Pollheimer1, Thomas Bauernhofer2, Peter Kornprat3,Richard A. Lindtner1, Andrea Schlemmer4, Peter Rehak5, and Cord Langner1

1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 Graz, Austria

2 Department of Internal Medicine, Division of Oncology, Medical University of Graz,Auenbruggerplatz 15, A-8036 Graz, Austria

3 Department of Surgery, Division of General Surgery, Medical University, AustriaAuenbruggerplatz 29, A-8036 Graz, Austria

4 Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Auenbruggerplatz 2, A-8036 Graz, Austria

5 Department of Surgery, Research Unit for Biomedical Engineering & Computing,Medical University of Graz, Auenbruggerplatz 29, A-8036 Graz, Austria

E-Mail address of corresponding author: [email protected] address of presenting author: [email protected]

Introduction:Targeted cancer therapy directed against tumor-promoting receptors represents asophisticated therapeutic approach. The human prolactin receptor (PRLR), a member of the Cytokine Receptor Superfamily, has been reported to promote tumour growth through an auto-/paracrine loop. However, the amount and clinicalsignificance of PRLR expression in colorectal cancer (CRC) remains to be elucidated.Our study aimed to evaluate the prevalence of PRLR in a large sample of CRC and tocorrelate findings with clinicopathological data as well as patient outcome. In addition, PRLR expression in local and distant metastases was compared with that ofcorresponding primary tumours.

Methods:400 patients were randomly sampled from the files of the CRC database of the Institute of Pathology, Medical University of Graz, Austria. Of these, 373 primary CRCand 171 corresponding metastases were evaluated for PRL-R expression by immuno-histochemistry using a tissue microarray technique. Follow-up data were availablefor 342 (91%) patients. Median follow-up was 59 months (mean 64, range 0-182).PRL-R expression was semiquantitatively scored as either focal (<10% of tumour cellspositive), moderate (10-50%), or extensive (>50%). PRLR expression was related tovarious clinicopathological parameters and to patient outcome.

Results:PRLR expression was observed in 360 (97%) primary tumours, with 21 (6%) casesshowing focal, 55 (15%) moderate and 284 (76%) extensive expression, respectively.Extensive PRLR expression was significantly associated with tumour size (p=0.002)and grade (p<0.001) as well as histological subtype, with classical adenocarcinomasshowing stronger PRLR expression than mucinous adenocarcinomas (p<0.001).Somer’s D coefficients for concordance of primary tumours with correspondinglymph node and distant metastases were D = 0.719 (p<0.001) and D = 0.535 (p=0.001),respectively.

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Abstract No 1/9

Regarding the whole group of tumours, extensive PRL-R expression predicted bothdisease progression as well as cancer-related death (p=0.08 each). Restricting analysis to high grade cancers, 43/73 (59%) patients with tumours showing extensive PRLR expression experienced disease progression compared with 11/33(33%) patients with tumours either lacking PRLR expression or showing onlyfocal/moderate expression (p=0.03). Similarly, 39/73 (53%) patients with tumoursshowing extensive PRL-R expression died of disease compared with 9/33 (27%) patients with tumours either lacking PRLR expression or showing only focal/moder-ate expression (p=0.04).

Discussion and Conclusion:PRLR expression is common in CRC, with high concordance between primary tumours and corresponding metastases. Extensive expression was significantly associated with tumour size, grade and histological subtype. In view of evolving targeted therapy strategies in CRC, widespread PRLR expression may offer an additional therapeutic perspective in affected patients.

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Abstract No 1/10

Aurora-kinase B expression is dependent on cell proliferationin breast carcinoma

Names and affiliations Katalin Hegyi, Zsuzsa Sándor, Kristóf Egervári, László Sarkadi,Gábor MéhesDepartment of Pathology, University of Debrecen, Debrecen, Hungary

E-Mail address of presenter: [email protected]

Introduction: Chromosomal instability and formation of aneuploidy are key features of the malignant phenotype. Deregulation of the components of the mitotic apparatus maysignificantly contribute to errors of the cell division and by that, to tumor aggres-siveness. Aurora-B (AuB) is a mitotic kinase which acts as a part of the chromosomalpassenger complex essential for chromosome segregation. During normal cell cyclethe Aurora B kinase is expressed in late G2 and M phase and remains active in theprocess of mitosis. Overexpression of AuB was reported in different conditions including aggressive lymphomas, breast carcinoma and colorectal carcinoma. However, systemic evaluation of AuB expression in relation to the cell cycle was notperformed so far. In our study we addressed this issue by the parallel estimation ofthe AuB expressing G2/M fraction and the proliferative fraction of breast cancercases.

Methods: 33 cases of invasive ductal and lobular breast carcinomas were examined immuno-histochemically for the AuB and the Mib-1 cell proliferation fraction to define the potential overexpression and increased or delayed effect of the kinase activity intumor cells. The immunopositive cells were determined semiquantitatively in percentage of the total tumor cell fraction. In addition, chromosome 17 copy numberand the Her-2 gene status was also determined by FISH analysis.

Results:AuB expression was found in the range of 0 to 35 %, (mean=7.7, SD±10.1) with a subset of breast carcinomas showing highly elevated AuB expression. Cell prolifera-tion capacity (Mib-1 index) of the same tumors was between 1 and 95 % (mean=22.6,SD±23.6). Interestingly, a strong correlation was found between the AuB and Mib-1positive fraction (r=0.75), suggesting, that increased expression of AuB is a featureof tumors with high proliferative fractions. Breast carcinomas with Her-2 amplifica-tion presented with a significantly elevated AuB fraction (p=0.05) but they alsoshowed higher Mib-1 proliferation index. Discussion and Conclusion: In conclusion,the mitotic kinase AuB is well detectable by immunohistochemistry under routineconditions. The rate of AuB expression proved to be dependent on the proliferativefraction of the tumor. To obtain an accurate picture on AuB overexpression in proliferating cell populations the AuB/MiB-1 index also considering the increase inthe G2/M cell fractions in proliferating cell populations is proposed.

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Abstract No 2/1

The role of Lim1 in renal development and renal neoplasms

Names and affiliation: Nusshold E1, Senenayake U1, Guelly C2, Ebner B2, Leuschner I3,Höfler G1, Gürtl B1

1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 Graz

2 Centre of Medical Research, Medical University of Graz, Stiftingtalstrasse 24, A-8010 Graz

3 Kiel Pediatric Tumor Registry, Institute of Pathology, Christian Albrechts University Kiel, Michaelisstr. 11, D-24105 Kiel

E-Mail address of presenter: [email protected]

Introduction: Lim1 encodes a LIM class homeodomain transcription factor, which plays an important role in the mesenchymal-epithelial transition during kidney developmentof mouse and rat. Inactivation of Lim1 in nephric duct tissue leads to development ofsmaller kidneys, hydronephrosis and hydroureter, indicating abnormal formation ofdistal ureter. In our study we investigated the role of Lim1 during normal human kidney develop-ment, cystic renal maldevelopment and different renal neoplasms. We also analysedcharacteristics of Lim1 further in a cell culture model.

Methods: Immunohistchemistry was performed on paraffin-embedded samples of fetal kidneysof different gestational ages, multicystic dysplastic kidneys and different renal neoplasms.Lim1 was overexpressed in HEK-293 cells by transfection of a vector containing thecoding sequence of Lim1. Changes in gene expression was analysed by qRT-PCR andimmunohistochemistry, influence on the cell cycle by FACS analysis.

Results: In our samples we identified so far expression of Lim1 beginning at 10 weeks of gestation in S-shaped and comma shaped bodies. At a later gestational age someimmature glomeruli also showed positivity for Lim1. So far analysis of renal neoplasms revealed expression of Lim1 in some cases of nephroblastomas, but nonein renal cell carcinomas. Cell culture experiments so far indicated that overexpressionof Lim1 was sufficient to enhance gene expression of an epithelial phenotype.Discussion and Conclusion: Our study indicates that Lim1 is expressed during humanrenal development and downregulated in mature kidney. In embryonal tumors of thekidney reactivation can be observed suggesting a possible oncogenic role of thistranscription factor.

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Abstract No 2/2

Intrauterine fetal death during the 3rd trimenon-impact of placental findings

Names and affiliations: Gibiser K1,2, Holzapfel-Bauer M2, Haas J2, Guertl-Lackner B1.

1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036Graz

2 Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, A-8036 Graz

E-Mail address of presenter: [email protected]

Introduction:Intrauterine fetal death (IUFD) is an immense burden for every person involved.Therefore it is very important to identify the different fetal, maternal and placentalcauses for IUFD. A better knowledge about the correlation of the risks would makebetter counselling of parents possible and might prevent such events. In our study weare not only assessing fetal and maternal risk factors, but we also investigate macroscopic and histological findings of the placenta, which cannot be identified onultrasound.

Methods:In a retrospective study 65 IUFDs from the 28th week till term were included. Investigated maternal risks are age, BMI, diabetes, hypertension, earlier pregnan-cies, HELLP, smoking and (pre-) eclampsia. Fetal parameters include weight, ultra-sound biometry, twins, umbilical cord complications, quantity of the amniotic fluidand underlying syndromes. Macroscopic and histological findings of the placenta including status of maturation are compared as well.

Results:So far 13 placentas among all the samples investigated showed inappropriate maturation of chorionic villi compared to gestational age. 10 placentas had a trimmedweight beneath the 10 percentile. 6 placentas had not only delayed maturation ofchorionic villi, but also a low placental weight.

Discussion and Conclusion:So far in the literature maternal risk factors such as hypertension and eclampsiahave been widely investigated in different studies, whereas placental morphology asan independent risk factor has not been investigated in detail. Our study indicatesthat low placental weight and inappropriate maturation might play a role in IUFD.

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Abstract No 2/3

The prognostic value of p16 and p27 in recurrent low and highgrade bladder cancer

Names and affiliations: Vollbrecht Claudia1, Steiner H2, Schaefer G1, Steiner E2, Brunner A1

1 Institute of Pathology, Medical University of Innsbruck2 Department of Urology, Medical University of Innsbruck

E-Mail address of presenter: [email protected]

Introduction: We investigated the value of expression and distribution pattern of p16, p27 in superficial bladder cancer in correlation with p53, Ki-67 and CK20 and clinical-patho-logical parameters.

Methods: Primary and recurrent urothelial carcinomas of 31 patients were evaluated for the expression of p16, p27, Ki67, p53, and CK20 by means of immunohistochemistry.Specimens were analyzed using a scoring system (range 0 – 12) including percentageof positive cells and intensity of staining. In addition the localization of positivelystained cells within each tumor was evaluated taking into account the localization ofstaining in basal, intermediate and/or superficial cells. In addion FISH fpr 9p21(p16)was performed in selceted cases including different p16 expression patterns.

Results:A total of 107 tumors was analysed. The expression of p16 and p27 correlated significantly with grade (p<0.001 and p=0.02) as well as with expression of p53(p<0.001 for both) and ki67 (p=0.02 and p<0.001). Both, p16 and p27 were mostly found in a patchy distribution. While p16 staining wasmainly found in basal and intermediate cell layers, p27 was mostly found in the superficial cell layers. Comparing the expression pattern of different markers, astrong an homogenoeus expression was restricted to high grade tumors, while in lowgrade tumors a more heterogeneous expression pattern was noted. The recurrenttumors of the patients mostly showed a similar expression pattern than the primarytumor.

Discussion and Conclusion: p16 and p27 are differentially expressed in low and high grade bladder cancer suggesting an association with the degree of differentiation.

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Abstract No 2/4

Distribution of HPV genotypes in penile squamous cell carcinomas

Stephan Sygulla*, Sebastian Mannweiler*, Yas Razmara**, Karl Pummer**, Sigrid Regauer*

*Institut für Pathologie, **Universitätsklinikum für Urologie, Medizinische Universität Graz, A-8036 Graz

BackgroundPenile squamous cell carcinomas (SCC) are either human papilloma virus (HPV) induced or arise in the background of dermatoses. In contrast to carcinomas of theuterine cervix (nearly in 100% HPV-induced) and vulvar SCC (about 30% HPV-induced) the prevalence of HPV and dermatoses in penile SCC is not exactlyknown.

Material and MethodsWe analyzed retrospectively 95 archival penile surgical specimens (28 foreskins, 21excisions of glans penis and 46 penectomies) from the Institute of Pathology, Medical University Graz, Styria, Austria. 18 in-situ SCC and 77 invasive SCC (TNM2002: 63/95=66% pT1, 9/95 = 9% pT2, 5/95 = 5% pT3) were analyzed by immuno-histochemistry with antibodies to p16 („surrogate marker“ for transforming HPV- infection) and 85 of these 95 penile SCC were additionally analyzed with molecular methods for 27 HPV-low risk und HPV high-risk genotypes (InnogeneticsLIPA HPV-Genotyping)

Results65 of 95 (68%) penile SCC were p16-positiv, 30/95 (32%) were p16-negative. All p16-negative SCC were also negative for HPV after genotyping. For 55 of the 65 p16- positive SCC genotype analysis was available: 48/55 SCC (87%) harboured HPV16genotype as a single genotype and in 2/55 SCC (3.6%) HPV 45 was identified as thesingle genotype. HPV 18 was not identified as a single genotype, but present in 2/5SCC with multiple HPV-high risk genotypes. In total, only 5/55 (9%) SCC harbouredmore than one HPV genotypes: in 2 SCC HPV-18 was detected together with HPV 31and 58, and 3 SCC HPV 31, 33, 51 and 66.

Conclusions30% of penile SCC are HPV-negative and associated with lichen sclerosus or lichenplanus. About 2/3 of the examined penile SCC in Styria are HPV-induced and in over90% HPV16 is the sole genotype. HPV18 was not detected as a single HPV-genotypein penile SCC, only in infections with multiple HPV-high-risk and low-risk genotypes.The prevalence of HPV in penile SCC is higher than in vulvar SCC but lower than incervical uterine carcinomas. HPV-vaccination could prevent a significant percentageof penile SCC.

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Abstract No 2/5

Nephrogenic rests – genetic precursor lesions of nephroblastomas?

Names and affiliations: Senanayake U1, Flicker K2, Obenauf AC2, Speicher MR2,Leuschner I3, Höfler G1, Gürtl B1. 1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25,

A-8036 Graz2 Institute of Human Genetics, Medical University of Graz, Harrachgasse 21/8,

A-8010 Graz3 Kiel Pediatric Tumor Registry, Institute of Pathology,

Christian Albrechts University Kiel, Michaelisstr. 11, D-24105 Kiel

E-Mail address of presenter: [email protected]

Introduction:Nephroblastomas are embryonal renal neoplasms. Currently nephrogenic rests areconsidered as precursor lesions of nephroblastomas. In our study we investigatedthe genetic relationship between intralobar nephrogenic rests and nephroblastomascomparing genetic changes by array CGH.

Methods:Manual microdissection was performed to isolate blastemal and epithelial regions ofnephroblastomas and nephrogenic rests. 250ng genomic DNA and reference DNAwere differentially labelled with dCTP-Cy5 and dCTP-Cy3, respectively and co-hybridized on a 8x60 K array platform. Slides were scanned using Agilent’s microarray scanner G2505B and analyzed using Agilent DNA Analytics software4.0.76.

Results:Analysis of 7 nephroblastomas and 9 nephrogenic rests revealed partial gains ofchromosome 1, chromosome 12, chromosome 16 and chromosome 17 in nephroblas-tomas. There was no difference in genetic aberrations between blastemal and epithelial regions. Nephrogenic rests also showed gains of the same chromosomal regions in the identical chromosomes, additionally, gains of chromosome 22 and partial deletions of chromosomes 13 and 16.

Discussion and Conclusion: Our data demonstrate, as already described for perilobar nephrogenic rests, addi-tional genetic changes in intralobar nephrogenic rests compared to correspondingnephroblastomas. These results indicate that oncogenic transformation might notapply to all nephrogenic rests.

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Abstract No 2/6

Six2 – embryonically active transcription factor with oncogenic properties?

Names and affiliations: Senanayake U1, Suman D1, Leuschner I2, Schauer S1, Vesely P1, Höfler G1, Gürtl B1.1 Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25,

A-8036 Graz2 Kiel Pediatric Tumor Registry, Institute of Pathology,

Christian Albrechts University Kiel, Michaelisstr. 11, D-24105 Kiel

E-Mail address of presenter: [email protected]

Introduction:The morphology of nephroblastomas recapitulates embryonal kidney development.Comparison of gene expression patterns of fetal kidney and primary nephroblas-tomas indicated that blastema is in the stage of mesenchymal-epithelial transition.During kidney development metanephric mesenchyme also contains a renal progenitor cell population expressing Six2. In our study we investigated whetherblastema shows not only morphological but also genetical characteristics of progenitor kidney cells possibly influencing prognosis and treatment options.

Methods:Manual microdissection was carried out to separate morphologically distinct tumorareas of nephroblastomas. Up to 500 ng of total RNA were reverse transcribed intocDNA using the High Capacity cDNA reverse transcription kit (Applied Biosystems,UK). QRT-PCR was performed to analyse the mRNA expression of the Six2 gene relative to the housekeeping gene 18S.

Results:So far we analyzed samples of blastemal and epithelial areas from nephroblastomaswith various morphological subtypes. Blastemal regions showed a high level of mRNAexpression of Six2 in all cases of blastema rich tumors and 2 cases with mixed phenotype. One triphasic mixed tumor showed relatively similar expression in bothepithelial and blastemal regions. However, all epithelial regions investigated so farhad low expression of six2 compared to blastema.

Discussion and Conclusion:Our study shows that epithelial and blastemal areas even within the same tumor harbour a different genetic pattern. This might contribute to the divergent responseto chemotherapy and clinical course.

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Abstract No 2/7

Expression of ATGL is up-regulated in malignant tumors underhypoxic conditions

Names and affiliations: W. Alzoughbi, S. Das, S. Schauer, G. Gorkiewicz, T.K. Palaniappan, P. Vesely, B. Gürtl-Lackner and G. Höfler Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 GrazMail address of presenter: Wael Alzoughbi, Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, A-8036 Graz, Austria,

E-Mail address: [email protected]

Introduction: Lipid metabolism is established as a key factor in the pathophysiology of malignantgrowth. Under hypoxic conditions, malignant cells detoxify excess non-oxidized freefatty acids (FFA) via esterification into triglycerides (TG). Since adipose triglyceridelipase (ATGL) is the key enzyme for subsequent remobilization, we evaluated its roleunder hypoxic conditions.Methods: HT29 (adenocarcinoma, colon), HepG2 (hepatocellular carcinoma), U87-MG(glioblastoma) and HTB115 (leiomyosarcoma) cells were cultured under normoxic(20%) or hypoxic (1% oxygen) conditions in the presence or absence of Xanthohumol(XN), a diacylglycerol acyltransferse inhibitor. Lipids were analyzed by massspectrometry. ATGL and hormone-sensitive lipase (HSL) mRNA were determined byRT-PCR, protein by immunohistochemistry and lipase activity by FFA release fromTG.

Results: Under hypoxic conditions, ATGL mRNA expression was up-regulated in all the fourcell lines up to 2.1-fold. Increased levels of ATGL protein were detected in HTB115 cells.However, there was no significant increase in lipase activity. Interestingly, we detectedan increase in cytoplasmic TG (72%), but a decrease in diacylglycerol levels underhypoxia (64%) in HTB115 cells. HSL mRNA levels showed no significant differencesbetween normoxia and hypoxia in all cell lines. Importantly, cells treated with XN hadno increase in ATGL mRNA and showed decreased proliferation and increased celldeath.

Discussion and Conclusion:Up-regulation of ATGL on mRNA and protein level might be a consequence of TGaccumulation in malignant cells under hypoxic conditions. Why this up-regulation isnot accompanied by increased lipase activity resulting in TG conversion to DAG andFAA is currently being investigated. These mechanisms might indicate an importantrole for ATGL in the metabolism of malignant cells facilitating survival in a hostileenvironment.

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Abstract No 2/8

Dermatofibroma, a neoplastic or an inflammatory lesion?

Names and affiliations: Iva Brcic1, Luka Brcic2, Ivana Ilic1

1 Clinical Department of Pathology and Cytology, Clinical Medical Center Zagreb,Croatia

2 University of Zagreb, School of medicine, Zagreb, Croatia

E-Mail address of presenter: [email protected]

Introduction: Dermatofibroma (DF) is a frequent skin lesion which is often easily recognised clinically and histologically. However, the theory about the nature of DF is still not officially accepted.Langerhans cells (LC) are antigen-presenting cells that are, when compared to normal skin, more numerous in a spectrum of inflammatory skin lesion and less numerous in malignant tumours. The results are not so straightforward for benign tumours so we tried to see if the number of LC in DF points more toward inflamma-tory or neoplastic lesion.

Methods:From our archive we collected 20 skin biopsies from each leasion (postoperative scar,dermatofibroma and dermatofibrosarcomas) and retrospectively analyse them. Wecompared the number of intraepidermal LC over DF with the number of intraepidermalLC over scar and over DFS. For highlighting the LC in the epidermis CD1a antibody(clone OB-2; Dako, Glostrup, Denmark) were used. The intraepidermal CD1a+ cellswere enumerated as a percentage of 100 epidermal cells. At least two areas on highpower field were counted and mean +/- SD percentage was calculated in each specimen. Statistical analysis was preformed by nonparametric Mann-Whitney U test.Differences were considered to be significant at p<0.05.

Results:The number of intraepidermal LC above DF was found to be significantly lower thanthe number of LC in the epidermis above the scar (2.00+/-0.52 and 6.80+/-1.89;p<0.001). We also found significantly smaller number of intraepidermal LC in DFSwhen compared to the number of intraepidermal LC in a scar (2.76+/-1.18 and 6.64+/-1.86; p<0.001). There was no statistically significant difference between the numberof intraepidermal LC in DF and DFS (2.00+/-0.52 and 2.76+/-1.18; p=0.056).

Discussion and Conclusion:We used DFS as an example of neoplastic lesion and scar as a model for final phaseinflammatory lesion. Both lesions are morphologicaly similar to DF. The number of intraepidermal LC in DF is closer to the number of intradermal LC in DFS than to thescar. Based on the number of LC, DF is closely related to a neoplastic origin than toinflammatory reaction.

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Abstract No 2/9

Solid pseudopapillary tumors of the pancreas: a case series,comparison of histopathological and clinical data

Names and affiliations: S. Sunitsch1, J. Munding1, O. Belyaev2, W. Uhl2, A. Tannapfel1

1 Institut für Pathologie der Ruhr-Universität Bochum am Berufsgenossen-schaftlichen Universitätslinikum Bergmannsheil

2 Chirurgische Klinik St. Josef-Hospital, Klinikum der Ruhr-Universität Bochum

E-Mail address of presenter: [email protected]

Introduction: Solid pseudopapillary neoplasms (SPN) are rare pancreatic tumors, representing only1% to 2% of all pancreatic neoplasms, first described by Frantz in 1959. Frantz described three patients suffering from SPN, with solid and cystic components thatwere previously clinically misdiagnosed as nonfunctioning islet cell tumors. The factthat the tumor occurs predominantly in young women suggests that gender specificfactors may play a role, although it has also been reported in older and male patients.However, no concomitant data has been found until now.

Methods: The clinical course, pathohistological data and clinical outcome of four patients withSPN treated at Ruhr-Universität Bochum were described. Furthermore additional immunohistochemical and molecularbiological data is presented.

Results: From 2008 to 2009 four patients with SPN were diagnosed at our institution. Amongothers, this case series includes three female (age range 17-56 years) and one malepatients (26 years). Predominantly the tumors were localized in the corpus (one inthe head, two in the corpus and one in the tail of pancreas), with a mean diameter of3,6cm. All tumors exhibited K-ras wildtype. Immunohistochemistry including DPC4,ß-catenin, progesterone-receptor and synaptophysin was analysed, too.

Discussion and Conclusion: SPN are rare pancreatic neoplasms with low malignant potential found primarily inyoung women. Curative surgical resection may be performed safely to rule out malignancy. After complete resection of the tumor the prognosis is excellent. However preoperative diagnosis is difficult and cytological diagnosis is impossible.Histopathologically the SPN should be sepsrsted from endocrine tumors and acinarcarcinoma.

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